If the cells that make up your body are little factories, then the shipping department just picked up a Nobel Prize this morning with the award for physiology or medicine going to researchers Randy Schekman of the University of California at Berkeley, James Rothman of Yale University, and Thomas Südhof of Stanford.

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If the cells that make up your body are little factories, then the shipping department just picked up a Nobel Prize this morning with the award for physiology or medicine going to researchers Randy Schekman of the University of California at Berkeley, James Rothman of Yale University, and Thomas Südhof of Stanford. These scientists don't work together, but their research does overlap and play off each other in important ways. In fact, this isn't the first time some of these men have shared major research awards.

What makes their work so important? It's really all about increasing our understanding of how individual cells operate and participate in major bodily systems like immunity or hormone control. If you built little models of cells back in grade school, you probably have a mental image of them as a sort of lumpy sack with a couple of things inside — a big fat nucleus and some squirrelly little mitochondria, mostly. But it turns out that there's a lot more happening in the interior of a cell than that. Much of that activity is centered around vesicles — bubbles in the fluid that fills a cell. There are many different kinds of vesicles doing many different jobs, but one of the important things they do is move molecules, either within the cell or from the cell to the outside world.

Here's how the Nobel website explains it:

In a large and busy port, systems are required to ensure that the correct cargo is shipped to the correct destination at the right time. The cell, with its different compartments called organelles, faces a similar problem: cells produce molecules such as hormones, neurotransmitters, cytokines and enzymes that have to be delivered to other places inside the cell, or exported out of the cell, at exactly the right moment. Timing and location are everything. Miniature bubble-like vesicles, surrounded by membranes, shuttle the cargo between organelles or fuse with the outer membrane of the cell and release their cargo to the outside. This is of major importance, as it triggers nerve activation in the case of transmitter substances, or controls metabolism in the case of hormones. How do these vesicles know where and when to deliver their cargo?

The "how" question is really what Schekman, Rothman, and Südhof's work is all about. By examining what happened in cells where this shipping system wasn't working properly, they were able to figure out how different parts of the system were actually supposed to be operating and were able to learn more about the genetic and environmental factors that can throw the cellular shipping department off its game. What they've learned is having a big impact on how researchers think about immune system disorders, diabetes (insulin is one of the chemicals that vesicles move around), and neurological problems linked to hormone transport.

This chart describes the key problem with being Batman — it doesn't take a serious injury to seriously disable you. Your body can rack up big damage over years of repeated small stresses and strains — jumping from roof to roof two or three times a week, for instance, or slamming your knuckles into a bad guy's face every night.

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This chart describes the key problem with being Batman — it doesn't take a serious injury to seriously disable you. Your body can rack up big damage over years of repeated small stresses and strains — jumping from roof to roof two or three times a week, for instance, or slamming your knuckles into a bad guy's face every night.

Neuroscientist and kinesiologist Paul literally wrote the book on what it would take to create a non-superhuman superhero, like Batman. In a post at Scientific American blogs, he explains the major physical impacts of being the Dark Knight. His big conclusion: Nobody could be Batman for very long. And even after they retired, they'd feel the echo of what they'd done to their body every day for the rest of their lives.

It’s hard to gauge the long-term effects of being exposed to these harsh occupations. Looking at NFL players provides another way to get at long term effects. In fact I used the very short average career—3-5 years—of NFL players as a way to estimate Batman’s longevity in Becoming Batman.

Skilled writer Peter King provided an in-depth expose on football players in the Dec 12, 2011 issue of Sports Illustrated. This piece was a follow up look at 39 members of the 1986 Cincinnati Bengals—25 years later—and spanned all forms of injury. But it’s the bodily injuries I want to focus on. In the category of “residual injury” over 70% had at least one surgery during their careers with ~40% having a post-NFL surgery for an injury related to football. Thirty percent had an upcoming surgery. More than 90% of the players said that they had lingering issues arising from an injury derived from their NFL careers.

Probably the most telling “statistic” is that on average these players reported 3 parts of the body that experienced pain each day. That’s a lot of injuries and a lot of discomfort.

Last week, an American and a Russian — Scott Kelly and Mikhail Kornienko — were selected to spend a year living continuously in space, aboard the International Space Station. Only four other people have done this before. All them were Russian, so Scott Kelly is going to break the American record for time spent in space.

The mission won't start until 2015, and it's part of a much longer term goal — sending people to Mars. We know that spending time in space does take a toll on the human body. For instance, hanging out without gravity means you aren't using your muscles, even the ones that you'd use to support your own weight on Earth. Without use, muscles deteriorate over time. Bone density also drops. Basically, after a few months in space, astronauts return to Earth as weak as little kittens. Which is, to say the least, a less than ideal situation for any future Mars explorers.

Having Kelly and Kornienko stay up for a year will give scientists more data on what happens to the human body in space, give them a chance to test out preventative treatments that could keep astronauts stronger, and allows them to see how the amount of time spent in space affects the amount of time it takes to physically recover from the trip. As an extra research bonus, Kelly is the identical twin brother of Mark Kelly, the astronaut married to former congresswoman Gabrielle Giffords. Which means that there will be a built-in control to compare Kelly to when he comes back from his mission.

In honor of that upcoming experiment, here's an old video that will give you an idea of what we knew (and didn't know) back at the dawn of the space age. Science in Action was a TV show produced by the California Academy of Sciences. In this 1956 episode, they explore the then-still-theoretical physiology of space travel ... with a special guest appearance by Chuck Yeager!

The Deep Sea News blog called it last week, but the official word from the experts is that this was the eye of a swordfish. The distinction is based on the size, the color, and the fact that there are bits of bone present around the edges (something you wouldn't see attached to a giant squid eye).

How do you get a swordfish eye without a swordfish attached? Simple: It's swordfish season. In the press release, Joan Herrera, curator of collections at the FWC’s Fish and Wildlife Research Institute in St. Petersburg, said that,
"Based on straight-line cuts visible around the eye, we believe it was removed by a fisherman and discarded."

But before we pack this mystery away, I think you should take one more close look at the giant eyeball, because it offers a great view a really interesting feature of fish eye anatomy. Fish eyes are similar to those of land-dwelling vertebrates. But there are some key differences. In particular, the shape of the lens...

In the human eye, you've got an iris, you've got an opening in the iris called the pupil, and you've got a flattish lens sitting behind the pupil. In a fish eye — including this one &mash; the lens is much more rounded and it sticks up through the pupil like a little nubbin.

A prominent characteristic of the fish eye, from the outside at least, is its bulbous nature. Some of the reasons for this will become apparent. The outer layer of the eye, the cornea, is dome-shaped and transparent. It is the first to receive light. With the terrestrial vertebrate eye, light travels through the air and hits the cornea. Because the air and cornea are of differing densities, the light is refracted (bent and directed) into the opening called the pupil. Water and cornea are of about equal densities so there is little refraction with the cornea of a fish eye. Again, with terrestrial vertebrates, the iris is the colored aperture that opens and closes, adjusting the size of the pupil and the amount of light entering the eye.

But in most teleost fishes, because of the protruding lens, the iris is rigid, making the pupil a fixed size. Therefore, to compensate for the amount of light entering the eye, an amount which could be too intense or not intense enough to measure, the retina adjusts the position of the photo receptors. And whereas our terrestrial eyes adjust to light levels within a few moments, fish eyes take much longer. We can observe this in aquarium fish that have been subjected to suddenly having their tank light turned on. Such fish typically hide until their eyes have adjusted to the light, which can take fifteen or twenty minutes.

The Nobel Prizes in science will be announced — one prize per day — between now and Wednesday. Today, the winners of the prize for physiology or medicine were announced.

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The Nobel Prizes in science will be announced — one prize per day — between now and Wednesday. Today, the winners of the prize for physiology or medicine were announced. John Gurdon and Shinya Yamanaka will share the award for work related to cloning and our ability to manipulate the functioning of stem cells.

What's interesting here is that the research these two men are winning the Nobel for happened nearly a generation apart. Gurdon's work was crucial to the development of cloning. You'll recall that some embryonic stem cells can grow up to be anything, any part of animal's living tissue. Differentiated stem cells, in contrast, are destined for a specific job — for instance, they could grow into skin cells, or nerve cells, but not both. In 1952, other scientists had concluded that you could take genetic material from a very early frog embryo, inject it into the egg cell of another frog, and get that to grow into a living animal — a clone. But those researchers thought this process would only work up to a point. They didn't think you could clone an adult, or even an older fetus. Gurdon proved them wrong. In a series of experiments published between 1958, 1962, 1966, he worked with older and older donor cells, and produced more developed clones — eventually growing fully adult, fertile frogs from cells taken from the intestines of tadpoles.

Yamanaka, meanwhile, did his research in the early part of the 21st century, developing the methods that allow us to trick grown-up, set-in-their-ways cells into behaving more like embryonic stem cells. Yamanaka's work is linked to Gurdon's because it explains why Gurdon (and researchers after him) were able to successfully clone adult animals from cells that had fully differentiated.

The research history here is a little hard to follow, especially with Gurdon's work. The description of his findings I have here is what I've been able to piece together from several different sources, citing several different dates and specific achievements. To help cut through some of the confusion, here's a couple of links where you can get a good, reasonably detailed idea of what this research is, and why it matters:

]]>http://boingboing.net/2012/10/08/the-2012-nobel-prize-in-physio.html/feed2Why do Olympic records keep getting broken?http://boingboing.net/2012/08/10/why-do-olympic-records-keep-ge.html
http://boingboing.net/2012/08/10/why-do-olympic-records-keep-ge.html#commentsFri, 10 Aug 2012 21:58:21 +0000http://boingboing.net/?p=175972Over at Discovery News, Emily Sohn asks the question I've been wondering for the last two weeks. Why are Olympians today better at their sports than Olympians of the past?]]>Over at Discovery News, Emily Sohn asks the question I've been wondering for the last two weeks. Why are Olympians today better at their sports than Olympians of the past? Why do speed records keep getting broken? Why can gymnasts do more elaborate routines?

I mean, I have plenty of reasonable, speculative answers for those questions. But I hadn't seen them addressed in a factual way. This is great. And fascinating.

The answer, experts say, involves a combination of incremental technological improvements, as well as a growing population of people attempting a larger variety of sports that they start earlier and stick with longer. The mind plays a big role, too, especially when it comes to toppling seemingly insurmountable barriers, like the four-minute mile of the past or the two-hour marathon of the future.

"There is almost certainly a species limit in terms of physical capabilities, and I suspect we might be in the range of that," said Carl Foster, an exercise physiologist at the University of Wisconsin, Lacrosse. "But every time scientists say humans are not going to go any faster, they've been shown to be wrong. You can take that one to the bank."

Through calculations of maximum power output, oxygen use, heart function and other factors, some researchers have attempted to predict what the absolute limits of human ability will be. Much-debated estimates include 1:58 for the marathon (a five-minute improvement over the current men's record of 2:03.38), and 9.48 for the men's 100m.